Interactions between inhalant allergen extracts and airway epithelial cells: Effect on cytokine production and cell detachment

被引:93
作者
Tomee, JFC
van Weissenbruch, R
de Monchy, JGR
Kauffman, HF
机构
[1] Univ Groningen Hosp, Dept Allergol, Clin Internal Med, NL-9713 GZ Groningen, Netherlands
[2] Univ Groningen Hosp, Dept Otorhinolaryngol, Groningen, Netherlands
关键词
airway epithelial cells; asthma; rhinitis; mites; pollens; protease activity; Dermatophagoides pteronyssinus; Lepidoglyphus destructor; Pleum pratensis; Betula verrucosa;
D O I
10.1016/S0091-6749(98)70057-0
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Background: The factors responsible for inducing or maintaining airway inflammation are poorly understood. Various studies have focussed on the mechanisms leading to allergic airway inflammation in patients with asthma and rhinitis. The observation of local airway inflammation in nonallergic patients with asthma ol rhinitis, including those with nasal polyposis, suggest that non-IgE-related mechanisms exist that may Lead to airway inflammation. Various lines of evidence suggest that epithelial cells may participate in local inflammation of the airways. Objective: This study focused on the interaction of airway epithelial cells with clinically relevant inhalant allergen extracts in vitro. Methods: Cultures of airway epithelial cells were exposed to mite, Timothy grass pollen, and birch pollen extracts. Production of IL-8, IL-6, monocyte-chemotactic protein-1 (MCP-1), and granulocyte-macrophage colony-stimulating factor and cell detachment were monitored while protease inhibitors and chromatography techniques were applied to identify the factors responsible fur these effects. Results: With the mite extracts, cytokine production and cell detachment was largely dependent on protease activity. With the pollen extracts, cytokine production without cell detachment seemed to be independent of protease activity. Conclusion: These findings support the view that epithelial cells may contribute to the pathogenesis of airway disease by their interaction with inhalant allergen extracts. Furthermore, allergen extracts may enhance airway inflammation by means other than their IgE-binding activity through both protease-dependent and protease-independent mechanisms.
引用
收藏
页码:75 / 85
页数:11
相关论文
共 44 条
[1]  
Bufe A, 1996, PLANTA, V199, P413, DOI 10.1007/BF00195733
[2]   MAJOR ALLERGEN PHL-P-VB IN TIMOTHY-GRASS IS A NOVEL POLLEN RNASE [J].
BUFE, A ;
SCHRAMM, G ;
KEOWN, MB ;
SCHLAAK, M ;
BECKER, WM .
FEBS LETTERS, 1995, 363 (1-2) :6-12
[3]  
CAMPBELL AM, 1994, IMMUNOLOGY, V82, P506
[4]   SEQUENCE-ANALYSIS OF CDNA CODING FOR A MAJOR HOUSE DUST MITE ALLERGEN, DER-P-1 HOMOLOGY WITH CYSTEINE PROTEASES [J].
CHUA, KY ;
STEWART, GA ;
THOMAS, WR ;
SIMPSON, RJ ;
DILWORTH, RJ ;
PLOZZA, TM ;
TURNER, KJ .
JOURNAL OF EXPERIMENTAL MEDICINE, 1988, 167 (01) :175-182
[5]  
DEMONCHY JGR, 1985, AM REV RESPIR DIS, V131, P373
[6]   Association of skin test reactivity, specific IgE, total IgE, and eosinophils with nasal symptoms in a community-based population study [J].
Droste, JHJ ;
Kerkhof, M ;
deMonchy, JGR ;
Schouten, JP ;
Rijcken, B .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1996, 97 (04) :922-932
[7]   Cellular and mediator responses twenty-four hours after local endobronchial allergen challenge of asthmatic airways [J].
Frew, AJ ;
StPierre, J ;
Teran, LM ;
Trefilieff, A ;
Madden, J ;
Peroni, D ;
Bodey, KM ;
Walls, AF ;
Howarth, PH ;
Carroll, MP ;
Holgate, ST .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1996, 98 (01) :133-143
[8]   AUGMENTATION OF PERMEABILITY IN THE BRONCHIAL EPITHELIUM BY THE HOUSE-DUST MITE ALLERGEN DER P1 [J].
HERBERT, CA ;
KING, CM ;
RING, PC ;
HOLGATE, ST ;
STEWART, GA ;
THOMPSON, PJ ;
ROBINSON, C .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1995, 12 (04) :369-378
[9]   A MAJOR HOUSE-DUST MITE ALLERGEN DISRUPTS THE IMMUNOGLOBULIN-E NETWORK BY SELECTIVELY CLEAVING CD23 - INNATE PROTECTION BY ANTIPROTEASES [J].
HEWITT, CRA ;
BROWN, AP ;
HART, BJ ;
PRITCHARD, DI .
JOURNAL OF EXPERIMENTAL MEDICINE, 1995, 182 (05) :1537-1544
[10]  
HUFFNAGLE GB, 1995, J IMMUNOL, V155, P4790